The two major categories of bloodstream infections are intravascular (those that originate within the cardiovascular system) and extravascular (those that result from bacteria entering the blood circulation through the lymphatic system from another site of infection). Of note, other organisms, such as fungi, may also cause intravascular or extravascular infections. However, because bacteria account for the majority of significant vascular infections, these types of bloodstream infections are dis cussed in more detail. Factors contributing to the initiation of bloodstream infections are immunosuppressive agents, widespread use of broad-spectrum antibiotics that suppress the normal flora and allow the emergence of resistant strains of bacteria, invasive procedures allowing bacteria access to the interior of the host, more extensive surgical procedures, and prolonged survival of debilitated and seriously ill patients.

Intravascular Infections

Intravascular infections include infective endocarditis, mycotic aneurysm, suppurative thrombophlebitis, and intravenous (IV), catheter-associated bacteremia. Because these infections are within the vascular system, organisms are present in the bloodstream at a fairly constant rate (i.e., a continuous bacteremia). These infections in the cardiovascular system are extremely serious and considered life threatening.

Infective Endocarditis. The development of infective endocarditis (infection of the endocardium most commonly caused by bacteria) is believed to involve several independent events. Cardiac abnormalities, such as con genital valvular diseases that lead to turbulence in blood f low or direct trauma from IV catheters, can damage cardiac endothelium. This damage to the endothelial surface results in the deposition of platelets and fibrin. If bacteria transiently gain access to the bloodstream (this can occur after an innocuous procedure such as brushing the teeth) after alteration of the capillary endothelial cells, the organisms may stick to and then colonize the damaged cardiac endothelial cell surface. After colonization, the surface will rapidly be covered with a protective layer of fibrin and platelets. This protective environment is favorable to further bacterial multiplication. This web of platelets, fibrin, inflammatory cells, and entrapped organisms is called a vegetation (Figure 1). The resulting vegetations ultimately seed bacteria into the blood at a slow but constant rate.

Fig1. Vegetations of bacterial endocarditis. Arrow indicates the vegetations. (Courtesy Celeste N. Powers, MD, PhD, Virginia Commonwealth University Medical Center, Medical College of Virginia Campus, Richmond, Va.)

The primary causes of infective endocarditis are the viridans streptococci, comprising several species (Box 1). These organisms are normal inhabitants of the oral cavity, often gaining entrance to the bloodstream as a result of gingivitis, periodontitis, or dental manipulation. Heart valves, especially those previously damaged, present convenient surfaces for attachment of these bacteria. Streptococcus sanguis and Streptococcus mutans are frequently isolated in streptococcal endocarditis. Gram-negative bacilli, known as the AACEK group, Aggregatibacter aphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae, can also be associated with endocarditis.

Box1. Agents of Infective Endocarditis

With the ever-increasing use of IV catheters, arterial lines, and vascular prostheses, organisms considered normal or hospital-acquired inhabitants of the human skin are able to gain access to the bloodstream and attach to various surfaces, including heart valves and vascular endothelium. It has been estimated that more than 200,000 nosocomial infections (bloodstream) occur annually in the United States in adults and children. The majority of these infections are caused by the use of intra vascular catheters. Staphylococcus epidermidis and other coagulase-negative staphylococci have been increasingly implicated as the cause of infection associated with intra vascular catheters. S. epidermidis is the most common etiologic agent identified in prosthetic valve endocarditis, with S. aureus being the second most common. S. aureus is an important cause of septicemia without endocarditis and is found in association with other foci, such as abscesses, wound infections, and pneumonia, as well as sepsis related to indwelling intravascular catheters.

Mycotic Aneurysm and Suppurative Thrombophlebitis. Two other intravascular infections, mycotic aneurysms and suppurative thrombophlebitis, result from damage to the endothelial cells lining blood vessels. With respect to mycotic aneurysm, an infection causes inflammatory damage and weakening of an arterial wall; this weakening causes a bulging of the arterial wall (i.e., aneurysm) that can eventually rupture. The etiologic agents are similar to those that cause endocarditis.

Suppurative thrombophlebitis is an inflammation of a vein wall. The pathogenesis of this intravascular infection involves an alteration in the vein’s endothelial lining followed by clot formation. The site is then seeded with organisms, thereby establishing a primary site of infection. Suppurative thrombophlebitis represents a frequent complication of hospitalized patients caused by the increasing use of IV catheters.

Intravenous Catheter–Associated Bacteremia. IV catheters are an integral part of the care for many hospitalized patients. More than 3 million central venous catheters are used annually in the United States. For example, central venous catheters are used to administer fluids, blood products, medications, antibiotics, and nutrition, and for hemodynamic monitoring. A short term, triple-lumen (channel opening within a tube) central venous catheter is shown in Figure 2. Unfortunately, a major consequence of these medical devices is colonization of the catheter by either bacteria or fungi, which can lead to catheter infection and serious blood stream infection. This consequence is a major nosocomial source of illness and even death.

Fig2. Short-term, triple-lumen central venous catheter. The ends from which the catheter is accessed are usually referred to as the hubs. After the catheter is inserted, the tip resides within the bloodstream.

IV catheter–associated bacteremia (or fungemia) is believed to occur primarily by two routes (Figure 3). The first route involves the movement of organisms from the catheter entry site through the patient’s skin and down the external surface of the catheter to the catheter tip within the bloodstream. After arriving at the tip, the organisms multiply and may cause a bacteremia. The second way that IV catheter–associated bacteremia may occur is by migration of organisms along the inside of the catheter (the lumen) to the catheter tip. The catheter’s hub, where tubing connects into the IV catheter, is considered the site at which organisms gain access to the patient’s bloodstream through the catheter lumen. The most common etiologic agents for IV catheter–associated bloodstream infections, regard less of the route of infection, are organisms found on the skin (Box 2). Certain strains of S. epidermidis appear to be uniquely suited for causing catheter related infections because of their ability to produce a biofilm or “slime” that consists of complex sugars (poly saccharides) believed to help the organism adhere to the catheter’s surface. The initial attachment of S. epidermidis to the catheter’s polystyrene surface is related to a cell surface protein. Once attached, the organism proliferates, subsequently forming a biofilm. Uncommon routes of IV catheter–tip infection include contaminated fluids or blood-borne seeding from another infection site.

Fig3. Possible routes by which microorganisms gain access to the bloodstream to cause intravenous catheter–associated bacteremias. (Modified from Elliott TS: PHLS Communicable disease report: line-associated bacteremias, CDR Review 3:R91, 1993.)

Box2. Common Agents of IV  Catheter–Associated Bacteremia

Extravascular Infections

Except for intravascular infections, bacteria usually enter the circulation through the lymphatic system. Most cases of clinically significant bacteremia are a result of extra vascular infection. When organisms multiply at a local site of infection such as the lung, they are drained by the lymphatics and reach the bloodstream. In most individuals, organisms in the bloodstream are effectively and rapidly removed by the reticuloendothelial system in the liver, spleen, and bone marrow and by circulating phagocytic cells. Depending on the extent of immunologic control of the infection, the organism may be circulated more widely, thereby causing a bacteremia or fungemia.

The most common portals of entry for bacteremia are the genitourinary tract (25%), respiratory tract (20%), abscesses (10%), surgical wound infections (5%), biliary tract (5%), miscellaneous sites (10%), and uncertain sites (25%). For the most part, the probability of bacteremia occurring from an extravascular site depends on the site of infection, its severity, and the organism. For example, any organism producing meningitis is likely to produce bacteremia at the same time. Of importance, certain organisms causing extravascular infections commonly invade the bloodstream; some of these organisms are listed in Table 1. In addition to these organisms, a large number of other bacteria and fungi that cause extravascular infections are also capable of invading the bloodstream. Whether these organisms invade the bloodstream depends on the host’s ability to control the infection and the organism’s pathogenic potential. Some of the organisms associated with potential bloodstream infections from a localized site include members of the family Enterobacteriaceae, Streptococcus pneumoniae, Staphylococcus aureus, Neisseria gonorrhoeae, anaerobic cocci, Bacteroides, Clostridium, beta-hemolytic streptococci, and Pseudomonas. These are only some of the organisms frequently isolated from blood. Almost every known bacterial species and many fungal species have been implicated in extravascular bloodstream infections.

Table1. Organisms Commonly Associated with  Bloodstream Invasion from Extravascular Sites of Infection

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